Application of light to a tissue surface has been used in several medical treatments. For example, it is known to apply light to a tissue surface in order to heal a pathological state, to remove a stenosis in a blood vessel or for laser welding of tissues, for example in order to treat a rupture in a vessel wall or to perform an anastomosis of two blood vessels. It is also known to use application of light for tissue regeneration and therapy. For example low level laser irradiation in the visible to far-red range of the light spectrum has been shown clinically to accelerate wound healing in skin wounds, and reduce pain and inflammation in musculoskeletal disorders. The underlying mechanisms are initiating (biostimulating) processes such as collagen synthesis, cell proliferation, and reducing secretion of inflammatory markers. Gavish et al., Lasers in Surgery and Medicine (2006) 38:779-786, which is incorporated herein by reference, discloses that low level laser in vitro stimulates vascular smooth muscle cell proliferation and collagen synthesis, modulates the equilibrium between regulatory matrix remodeling enzymes, and inhibits pro-inflammatory IL-1-β gene expression.
U.S. Pat. No. 7,051,738 to Oron et al discloses an apparatus for applying light to the heart tissue for a biostimulative and cytoprotective effect. U.S. Pat. No. 5,370,608 to Sahota et al discloses a light angioplasty catheter for exposing the vessel wall to light from an intravascular approach for the prevention of restenosis.
U.S. Pat. No. 7,108,692 to Frenz et al discloses an apparatus for applying light to the interior surface of a vessel wall for laser welding of two vessels. Light generated by an extracorporeal light source is guided to the interior of the blood vessel to be treated by a light guide. A light deflector directs the light in a substantially radial fashion onto the vessel wall.
Abdominal Aortic Aneurysm (AAA) formation is an arteriosclerotic process characterized by marked disruption of the musculoelastic lamellar structure of the media. Extensive destruction of the elastic tissue is associated with marked inflammatory cell infiltration and progressive diminution in the number of viable smooth muscle cells. With time, and aggravated by contributory risk factors such as systolic hypertension, aneurysm growth occurs through a complicated, but insidious, imbalance between matrix protein production and degradation, favoring expansion, thereby increasing the risk of rupture of the weakened wall.
AAA is present in approximately 10% of individuals over the age of 65 years, with its frequency increasing as the proportion of elderly individuals in the general population continues to rise. It is widely known that the risk of rupture increases in approximate proportion to aneurysm size, which can be monitored by computed tomography (CT), ultrasound, or magnetic resonance imaging (MRI). The estimated risk of rupture ranges from 10-20% for an abdominal aneurysm 6-7 cm in diameter, to 30-50% if the maximum diameter is greater than 8 cm. Overall mortality from a ruptured AAA is greater than 90%.
Current forms of aneurysm treatment focus either on the open abdomen, surgical, graft-based repair or endovascular exclusion of the diseased segment of aorta with large, membrane-covered, e.g. Gortex covered stents. Both techniques have major side effects with potentially life-threatening consequences, particularly in patients of advanced age (the majority of patients) or others at high risk or compromised cardiac function.